Neuroprotection - Dr. Wei Yi - Preventing brain cells from running out of fuel


Dr. Wei Yi
McGill University
Basic Research Fellowship
Amount awarded over 2 years: $80,000

MPP regulates PINK1 function for neuronal survival

Most of our body’s cells contain mitochondria, small components crucial to ensuring that a cell obtains adenosine triphosphate (ATP), a molecule that provides essential chemical energy for biological functions. When mitochondria are damaged, a cell must remove them before they contaminate it, which can lead to cell death.

“It’s really important to get rid of these mitochondria so that the cell can continue to make use of ATP,” says Wei Yi, a post-doctoral fellow at McGill University’s Montreal Neurological Institute. “It’s a question of making the most of this vital resource.”

Yi focuses on how damaged mitochondria are handled by neurons carrying dopamine, the complex agent that codes signals for movement control in the brain.

She developed an interest in neurodegenerative diseases like Parkinson’s while studying for her PhD at the Chinese Academy of Sciences. “I am also interested in the aging population of China, where larger numbers of people are likely to be affected by these diseases.”

Like other cells, neurons regularly remove all kinds of waste material, including mitochondria. This process, known as autophagy, is a rapidly expanding frontier in many areas of medicine. In the case of damaged mitochondria, an enzyme called PINK1 identifies and isolates these components in preparation for disposal. However, in as many as half of patients suffering from early onset Parkinson disease, PINK1 is itself damaged. It can no longer direct the removal of mitochondria.

“When this happens PINK1 is not actually protecting the cells,” Yi says. “They can end up with bad mitochondria and they will die from a lack of energy.”

As part of learning more about this problem, her research has revealed another enzyme, called MPP, which appears to control PINK1.

“By understanding this mechanism, we can find the pathways that could activate them again,” she explains. “If we can determine the relationship between PINK1 and MPP, it will provide a new way of treating Parkinson disease.”